Open AccessRetracted: Administration of MS ‐275 Improves Cognitive Performance and Reduces Cell Death Following Traumatic Brain Injury in Rats
Author(s) -
Cao Peng,
Liang Yong,
Gao Xu,
Zhao MingGuang,
Liang GuoBiao
Publication year - 2013
Publication title -
cns neuroscience and therapeutics
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.403
H-Index - 69
eISSN - 1755-5949
pISSN - 1755-5930
DOI - 10.1111/cns.12082
Subject(s) - morris water navigation task , traumatic brain injury , neuroprotection , cresyl violet , hippocampus , medicine , neurodegeneration , anesthesia , pathology , psychiatry , staining , disease
Summary Aims The MS ‐275 is a selective inhibitor of class I histone deacetylases ( HDAC s), which has been reported as a potential strategy in some central nervous system diseases associated with neurodegeneration and disturbed learning. However, its role in traumatic brain injury is not well defined. In this study, we examined the behavioral–cognitive performance as well as histology outcome in adult rats to evaluate whether postinjury administration of MS ‐275 (15 and 45 mg/kg) would provide neuroprotection benefits and ameliorate cognitive deficits following fluid percussion injury. Methods Traumatic brain injury (˜2.15 ATM s) was produced using a fluid percussion device with the lateral orientation. MS ‐275 was administered (15 and 45 mg/kg) systemically once daily for 7 days starting at 30 min after lateral fluid percussion TBI . Acquisition of spatial learning and memory retention was assessed using the Morris water maze ( MWM ) on days 10–14 after TBI . Brain tissues were collected and stained with Fluoro‐Jade B histofluorescence (for degenerating neurons) at 24 h after injury and cresyl violet (for long‐term neuronal survival) on day 14 postinjury. Results Behavioral outcome after TBI revealed MS‐275 treatment groups, at all doses examined, performed significantly better in the Morris Water Maze ( P < 0.001). Acute histology analysis demonstrated that 45 mg/kg MS ‐275 significantly reduced the number of degenerating neurons in the ipsilateral CA 2–3 hippocampus at 24 h postinjury ( P = 0.007). There was a trend for MS ‐275 to increase the survival of neurons in the CA 2–3 hippocampus on 14 days after TBI ( P = 0.164). Conclusion Our present data highlight the fact that MS ‐275 may provide neuroprotective effect and improve cognitive performance after TBI . We concluded that MS ‐275 is a potential novel treatment and will have an ameliorative effect on some of the pathological features associated with TBI .